Etiology
Reproductive history has been associated with the incidence of fibrocystic breasts, suggesting that aberration in normal development and a higher cellular proliferation of the breast epithelium may contribute to fibrocystic changes. Nulliparity and late menopause may increase the risk of fibrocystic breast disease, whereas high parity may decrease the risk.[6] There is also an increased incidence with the use of estrogen-replacement therapy, whereas tamoxifen use decreases the prevalence of benign breast lesions by a factor of 1.7.[6] Therefore, endocrine factors have long been suspected, but no consistent pattern of measurable hormonal abnormalities has been documented.[7]
Pathophysiology
The association of fibrocystic changes of the breast with reproductive and hormonal factors is the most likely explanation for the cyclic nature of symptoms seen in a majority of patients. It is important to keep in mind that patients who have fibrocystic changes with lumpy breasts or breasts with nondiscrete nodules do not have breast disease.[8] These changes do not correlate with an increased risk of breast cancer; fibrocystic changes of the breast reflect a broad spectrum of conditions that carry different risks for future development of breast cancer.[1][2]
In a minority of patients, a progression to a high-risk and malignant phenotype is associated with the accumulation of genetic mutations. There is a correlation between the rate of proliferation, aneuploidy, and increases in estrogen-alpha receptor, transforming growth factor-alpha, and c-erbB-2 expression rate, and increases in p53 tumor antigen expression. There is also an association between the progression from normal breast tissue, ductal hyperplasia, and presence of atypia, to the development of carcinoma.[9] It is therefore important to classify patients with fibrocystic changes based on the histologic phenotype characterized by the evidence of proliferation and atypia.
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